Physical activity targeted at maximal lipid oxidation: a meta-analysis.

Exercise is recognized as a part of the management of obesity and diabetes. Various protocols of exercise are proposed for the management of obesity, diabetes, and other metabolic diseases. One of the strategies proposed by several authors is low intensity endurance training targeted at the level of maximal oxidation. Large series using this technique are lacking. Addressing this issue, we performed a meta-analysis of the studies on anthropometric measurements. From a database of 433 articles, 15 were selected, including 279 subjects with 6 different populations. Studies duration ranged from 2 months to 12 months. Concerning weight loss, in the intervention versus control analysis, five studies with 185 participants were included with a significant effect size favors exercise (P = 0.02) without significant heterogeneity (I(2) = 0.0%, P = 0.83). Further randomized controlled trials for comparing it with other exercise protocols and defining its dose effectiveness on large samples are needed.

Decreased fat oxidation during exercise in severe obstructive sleep apnoea syndrome.

AIM: To assess whether the severity of obstructive sleep apnoea syndrome (OSAS) is associated with altered fat oxidation (FO) during physical exercise in men with type 2 diabetes (T2DM) and/or the metabolic syndrome (MetS). METHODS: A total of 105 consecutive overweight or/and T2DM male patients were hospitalized for metabolic check-ups including bioimpedancemetry to measure lean body mass (LBM), standardized exercise calorimetry to assess FO, maximum fat oxidation (MFO) and carbohydrate oxidation (CHO), and OSAS screening using respiratory polygraphy. Twenty patients were classified as having severe OSAS, according to the apnoea/hypopnoea index (AHI), with greater than 30 events/h (mean AHI: 45.2±14.3 events/h). They were group-matched for age, BMI, and the presence of T2DM and/or MetS with two other OSAS groups: mild (AHI<15 events/h [n=20]; mean AHI: 8.8±4.5 events/h); and moderate (AHI>15 events/h and<30 events/h [n=20]; mean AHI: 23.7±4.2 events/h). RESULTS: MFO adjusted for LBM was severely decreased in the severe OSAS group (1.6±1.0 mg.min(-1).kgLM(-1)) compared with the moderate (2.5±0.9 mg.min(-1).kgLM(-1); P=0.008) and mild (2.9±0.8 mg.min(-1).kgLM(-1); P=0.003) groups. All exercise-intensity levels (20%, 30%, 40% and 60% of the theoretical maximum aerobic power) showed reduced FO levels between the severe and mild-to-moderate OSAS groups. However, no differences in CHO were seen at any level of exercise between groups. Pearson's correlation analysis showed that AHI and the oxygen desaturation index were negatively associated with MFO corrected for LBM (r=0.41 and r=0.37, respectively; P<0.005). CONCLUSION: OSAS severity is associated with altered FO during exercise.

Limited predictive value of the IDF definition of metabolic syndrome for the diagnosis of insulin resistance measured with the oral minimal model.

AIM: To assess the agreement of the NCEP ATP-III and the IDF definitions of metabolic syndrome and to determine their predictive values for the diagnosis of insulin resistance. METHODS: For this purpose, we recruited 150 subjects (94 women and 56 men) and determined the presence of metabolic syndrome using the NCEP-ATP III and IDF definitions. We evaluated their insulin sensitivity S(I) using Caumo's oral minimal model after a standardized hyperglucidic breakfast test. Subjects whose S(I) was in the lowest quartile were considered as insulin resistant. We then calculated sensitivity, specificity, positive and negative predictive values of both definitions for the diagnosis of insulin resistance. RESULTS: The prevalence of metabolic syndrome was 37.4% (NCEP-ATP III) and 40% (IDF). Agreement between the two definitions was 96%. Using NCEP-ATP III and IDF criteria for the identification of insulin resistant subjects, sensitivity was 55.3% and 63%, specificity was 68.8% and 67.8%, positive predictive value was 37.5% and 40%, negative predictive value was 81.9% and 84.5%, respectively. Positive predictive value increased with the number of criteria for both definitions. CONCLUSION: Whatever the definition, the scoring of metabolic syndrome is not a reliable tool for the individual diagnosis of insulin resistance, and is more useful for excluding this diagnosis.

Association of the FTO gene with obesity and the metabolic syndrome is independent of the IRS-2 gene in the female population of Southern France.

AIM: The objective of the present study was to investigate the genetic association of the fat-mass-and-obesity-associated (FTO) gene in obese women in the presence of the known influential role of the insulin receptor substrate 2 (IRS-2) gene. METHODS: This case-control study was carried out in the Languedoc-Roussillon region of France, and included lean control women (n=128), and women (n=119) of various degrees of obesity (body mass index [BMI] mean+/-S.D.: 39.3+/-7.4kg/m(2)) and a prevalence of 26.9% of the metabolic syndrome (MetS). For the FTO gene, genotyping was performed by sequence-specific oligonucleotide-polymerase chain reaction (SSO-PCR) on the single nucleotide polymorphism (SNP) rs1421085 (C/T) while, for IRS-2, the rs1805097 (G/A) corresponding to variant Gly1057Asp was genotyped by direct sequencing. RESULTS: The FTO gene (homozygous C/C) was significantly associated to both simple and morbid obesity (P<0.026 and P<0.0034, respectively), with odds-ratios (ORs) of 2.58 (95% CI: 1.1-6.0) and 4.1 (95% CI: 1.6-10.5), respectively, independent of IRS-2. MetS was also associated with FTO (P<0.032, OR: 3.1, 95% CI: 1.1-8.5), but not with IRS-2. Genotypes of FTO were correlated with insulin resistance, and homozygous C/C was positively correlated with an increase in insulin resistance over the value predicted by the increase in BMI. CONCLUSION: These data confirm the influential role of the FTO gene in obesity in the French female population and, in addition, revealed the role of FTO in insulin resistance and MetS. These effects appeared to be independent of IRS-2, which is directly involved in insulin action. This study may offer new insights into the genetic determinants of obesity and MetS in women.

Effects of acute exercise on insulin sensitivity, glucose effectiveness and disposition index in type 2 diabetic patients.

AIM: The aim of this work was to quantify the magnitude of changes in insulin sensitivity (S(I)) and glucose effectiveness (S(G)) in response to acute exercise in type 2 diabetic (T2D) patients, as previously studied in non-diabetic subjects. METHODS: Seven T2D patients and seven non-diabetic controls participated in the study. Two intravenous glucose tolerance tests (0.5 g/kg) with frequent blood sampling over 180 minutes and mathematical modelling were carried out in a randomized fashion, one at rest and the other immediately following 15 minutes of exercise at 50% of the maximum theoretical heart rate (HR(max)) followed by five minutes at 85% of the HR(max). S(I) and S(G) were calculated using Bergman's minimal model. RESULTS: After exercise, S(I) was increased by 773% (from 0.62+/-0.16 to 5.41+/-1.59 min(-1) x 10(-4)/(microU/mL) and even reached the zone of control values at rest (5.52+/-2.28), whereas S(G) remained unchanged. The disposition index acute insulin response (AIR(G)) x S(I) and the product of fasting insulin (I(B)) x S(I) also increased after exercise. CONCLUSION: A single bout of exercise at moderate intensity in type 2 diabetics did not improve S(G), but markedly improved the low S(I) values found in these patients, indicating that the acute effects of exercise on S(I) are quantitatively important in the interpretation of training-related S(I) changes and may even be therapeutically useful on their own. Surrogates such as homoeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) were not sensitive enough to detect this increase in S(I) and should probably be used with caution in the follow-up of exercise protocols in diabetic patients.

Exercise calorimetry in sedentary patients: procedures based on short 3 min steps underestimate carbohydrate oxidation and overestimate lipid oxidation.

OBJECTIVES: Among exercise calorimetry tests designed for calculating the respective part of carbohydrates and lipids oxidized at exercise, some use 6 min steps and others use 3 min steps. Is this last method, which has been validated in healthy subjects, still accurate in very sedentary patients, who need more time to reach a steady state in respiratory gas exchanges? METHODS: We compared data obtained with calorimetry (RER and indicators of substrate oxidation) performed on the 2nd-3rd min and the 5th-6th min of each step of a protocol using four 6-min submaximal steps in 17 sedentary subjects (mean age: 51 years) including seven type 2 diabetics and six obese persons. RESULTS: Respiratory exchange ratio (RER) measured with the 3 min steps procedure are well correlated with the 6 min procedure in sedentary patients (r=0.928). However, a Bland-Altman analysis indicated an average underestimation of RER with 3 min steps (-0.0138). Moreover, we observed an average underestimation of carbohydrate oxidation rates of 70.1 mg/min with the 3 min steps procedure. On the contrary, as to lipid oxidation, we measured an average overestimation of 16.2 mg/min. Furthermore, carbohydrate and lipid oxidation rates measured with the 3 min steps procedure are well correlated with the 6 min steps procedure. Moreover, there was an average overestimation of the point at cross over with 3 min steps (+3.29 Watts). For lipox max point (power at which the increase in lipid oxidation induced by the increasing workload reaches a maximum), we observed an average underestimation with 3 min steps (-1.88 Watt). Although the differences between respectively mean values in cross over point and lipox max point between the two protocols are weak, a Bland-Altman analysis indicated more relevant discrepancies in many subjects between the two protocols. CONCLUSION: In very sedentary patients undergoing such tests for targeting exercise prescription, the 3-min procedure appears to be too short for performing an accurate calorimetry and we rather recommend the protocol using 6-min steps.

[Late diagnosis of a McArdle disease's case (type V glycogenosis)]. / Diagnostic tardif d'une maladie de McArdle (glycogénose de type V).

McArdle's disease is a metabolic myopathy characterized by a myophosphorylase deficiency resulting in an inability to degrade glycogen stores. We report the case of a 48 years old patient who complained since adolescence of rest and exercise myalgias and presented a chronic increased plasma creatine kinase activity. First, a maximal exercise test was performed. This test demonstrated a quasi lack of rise of respiratory exchange ratio and of blood lactate, possibly due to a glycogenolytic/glycolytic pathway deficiency. Second, a biopsy of vastus lateralis muscle was performed using Bergström needle. As expected, the analysis of mitochondrial function was normal. The in vitro screening test of the glycogenolysis/glycolysis pathway showed a lack of lactate production in presence of glycogen substrate. The study of muscular metabolism of glycogen revealed a glycogen accumulation and a decrease of active and total phosphorylase activities. These data allowed us to diagnose a type V glycogenosis, or McArdle's disease. The patient appeared heterozygous for the most frequent mutation (p.R50X).

Lower ability to oxidize lipids in adult patients with growth hormone (GH) deficiency: reversal under GH treatment.

BACKGROUND: The aim of the study was to characterize lipid oxidation at exercise in adults with growth hormone deficiency (GHD) and to evaluate the effect of 6 and 12 months of GH replacement therapy on substrate carbohydrate (CHO) and lipid utilization at exercise. PATIENTS AND MEASUREMENTS: Twenty-five patients with GHD and 40 matched controls participated in the study. Ten of the 25 GH-deficient patients were treated with recombinant GH for 12 months. Anthropometric measurements and exercise calorimetry were performed before and after treatment. Maximal fat oxidation and the crossover point [that is the percentage of the theoretical maximal power (Wmax th) where CHO become the predominant fuel used for oxidation] were determined. RESULTS AND CONCLUSION: The GH-deficient patients exhibited a highly significant shift in the balance of substrate oxidation during exercise, towards a decrease in fat oxidation, and a shift towards lower intensities of the crossover (52 +/- 5.5%vs. 72.6 +/- 6.6% of Wmax th, P < 0.03) and maximal fat oxidation (131.04 +/- 14 vs. 234.4 +/- 30.1 mg/min, P < 0.03) in the GHD and control groups, respectively. However, GH treatment at 6 and 12 months partially reversed this defect, resulting in an increase (+83%, P < 0.001) in the maximal ability to oxidize fat during exercise. These findings are consistent with the hypothesis that a lack of GH reduces the ability to oxidize lipids during exercise and that GH treatment restores this muscular metabolic property.

[Quality of life in HIV-infected children and adolescents under highly active antiretroviral therapy: change over time, effects of age and familial context]. / Evolution de la qualité de vie des enfants et adolescents infectés par le virus de l'immunodéficience humaine (VIH) sous multithérapie antirétrovirale: effet de l'âge et du contexte familial.

OBJECTIVE: To evaluate Quality of life (QoL) of HIV-infected children under highly active antiretroviral therapies, and its change over 18 months. MATERIALS AND METHODS: QoL was evaluated by self-administred questionnaires (french versions of AUQUEI, OK-ado, and compilation of both) in 23 young living with HIV/AIDS (6-15 yrs), under antiretroviral multitherapies, and re-evaluated 18 months later in 19 of them. RESULTS: At baseline, QoL in HIV-infected children-adolescents was relatively good. The answers given to each items and the mean score from infected children were similar to those obtained in uninfected healthy children. Moreover, infected adolescents distinguished definitly from healthy adolescents, describing higher QoL. The mean satisfaction score from the whole group decreased between M0 and M18 (mainly in the youngests), and mainly concerned 3 fields (self-esteem, health and school) while their somatic health remained stable or improved. An effect of the familial context was also observed for these 3 fields. CONCLUSION: The progressive decline of QoL in HIV-infected children, and the surprising high and steady level of satisfaction over-time provided by the adolescents, underlined the frailty of this population and the need for a psychologic management associated to the medical follow-up. Such a multidisciplinary approach should take into account the preoccupations and difficulties of each age-class, those linked to the diagnosis itself, and to the familial or scolar contexts, in order to preserve QoL of this pediatric population, as far as possible, in a long term.

Substrate oxidation during exercise: type 2 diabetes is associated with a decrease in lipid oxidation and an earlier shift towards carbohydrate utilization.

OBJECTIVES: Exercise is a recommended treatment for type 2 diabetes but the actual pattern of metabolic adaptation to exercise in this disease is poorly known and not taken in account in the protocols used. Metabolic defects involved in the pathways of substrate oxidation were described in type 2 diabetes. We hypothesized that type 2 diabetes, regardless of age, gender, training status and weight, could influence by its own the balance of substrates at exercise. METHODS: 30 sedentary type 2 diabetic subjects and 38 sedentary matched control subjects were recruited. We used exercise calorimetry to determine lipid and carbohydrate oxidation rates. We calculated two parameters quantifying the balance of substrates induced by increasing exercise intensity: the maximal lipid oxidation point (PLipoxMax) and the Crossover point (COP), intensity from which the part of carbohydrate utilization providing energy becomes predominant on lipid oxidation. RESULTS: Lipid oxidation was lower in the diabetic group, independent of exercise intensity. PLipoxMax and COP were lower in the diabetic group [PLipoxMax=25.3+/-1.4% vs. 36.6+/-1.7% %Wmax (P<0.0001)] - COP =24.2+/-2.2% vs. 38.8+/-1.9% %Wmax (P<0.0001). CONCLUSIONS: Type 2 diabetes is associated with a decrease in lipid oxidation at exercise and a shift towards a predominance of carbohydrate oxidation for exercise intensities lower than in control subjects. Taking into account these alterations could provide a basis for personalizing training intensity.

Low intensity endurance exercise targeted for lipid oxidation improves body composition and insulin sensitivity in patients with the metabolic syndrome.

BACKGROUND: To investigate the effects of individualized training on the metabolic syndrome. METHODS: Twenty-eight patients, suffering from the metabolic syndrome were studied before and after 2 months of training and compared to eleven patients who did not follow any training. All the patients were overweight. Training was individualized at the point where fat oxidation was maximal (LIPOX(max)) as determined by calorimetry. RESULTS: The patients exhibited a significant reduction in body weight (- 2.6 +/- 0.7 kg; P=0.002), fat mass (- 1.55 +/- 0.5 kg; P=0.009), waist (- 3.53 +/- 1.3 cm; P<0.05) and hip (- 2.21 +/- 0.9 cm; P<0.05) circumferences, and improved the ability to oxidize lipids at exercise (crossover point: + 31.7 +/- 5.8 W; P<0.0001; LIPOX(max): + 23.5 +/- 5.6 W; P<0.0001; lipid oxidation: + 68.5 +/- 15.4 mg.min(-1); P=0.0001). No clear improvement in either lipid parameters or fibrinogen were observed. The surrogates of insulin sensitivity evidenced a decrease in insulin resistance: HOMA%S (software): + 72.93 +/- 32.64; p<0.05; HOMA-IR (simplified formula): - 2.42 +/- 1.07; P<0.05; QUICKI: + 0.02 +/- 0.004; P<0.01; SI=40/I: + 3.28 +/- 1.5; P<0.05. Significant correlations were found between changes in body weight and HOMA-IR and between changes in LIPOX(max) and QUICKI. CONCLUSIONS: Individualized aerobic training improves lipid oxidation, body composition and insulin resistance.

Serum levels of insulin-like growth factor-I (IGF-I), and IGF-binding proteins-1 and -3 in middle-aged and young athletes versus sedentary men: relationship with glucose disposal.

The goal of this study was to characterize the respective effects of aging and endurance training on serum insulin-like growth factor I (IGF-I), as well as IGF-binding proteins (IGFBP)-1 and -3 in relationship with glucose disposal. Thirty-two subjects (16 middle-aged men: 8 cyclists and 8 sedentary men; and 16 young men: 8 cyclists and 8 sedentary men) were compared in this study. Insulin sensitivity (SI) and glucose effectiveness (Sg) were assessed by the minimal model. Endurance training increased SI, Sg, and IGFBP-1 and -3 in both age groups (P<.05), but the older group showed a greater increase in SI and IGFBP-1 than the younger group (P<.05). IGF-I was increased only in the middle-aged trained men (P<.05). An effect of aging was found in the sedentary subjects, who presented lower IGF-I and SI (P<.05) when older. This effect disappeared with training since IGF-I and SI were nearly identical in young and middle-aged trained subjects. SI was correlated with IGFBP-1 (P<.01). These data suggest that (1) endurance training increases SI, Sg, and IGFBP-1 and -3 in men and, for SI and IGFBP-1, this increase becomes more pronounced with age; (2) endurance training may attenuate the aged-related decline in SI and IGF-I; and (3) IGFBP-1 may protect against the risk of hypoglycemia by counteracting the hypoglycemic effect of IGF-I in such situations of high SI.

The effects of intensive training on insulin-like growth factor I (IGF-I) and IGF binding proteins 1 and 3 in competitive cyclists: relationships with glucose disposal.

The aim of the present study was to determine whether 4 months of intensified training would result in modified plasma insulin-like growth factor I (IGF-I), insulin-like growth factor binding protein 1 (IGFBP-1) or IGFBP-3 in eight competitive cyclists and eight sedentary individuals and to define the relationships of these factors with glucose disposal. Insulin sensitivity and glucose effectiveness--that is, the fractional disappearance of glucose independent of any change in insulinaemia--were measured with the minimal model (mathematical analysis of frequently sampled intravenous glucose tolerance test). Both glucose effectiveness and insulin sensitivity were higher in the cyclists than in the sedentary individuals, but did not increase further with training. IGF-I was higher in the cyclists than in the sedentary group only after raining (P < 0.05). Plasma IGFBP-1 and IGFBP-3 increased after training (38 and 20%, respectively; P < 0.05) in the cyclists and were higher than in the sedentary individuals (P < 0.05). IGF-I was negatively correlated with insulin sensitivity before and after training (r = -0.66 and -0.67, respectively; P < 0.05) and IGFBP-1 was negatively correlated with glucose effectiveness before andafter training (r = -0.68 and -0.77, respectively; P < 0.05). Our results show that strenuous endurance training improves the somatotrope axis (growth hormone-IGF) and that IGFBP-1 may be involved in glucose homeostasis, possibly by limiting the exercise-induced increase in glucose disposal, in competitive cyclists.

Reduction of fat accumulation and lipid disorders by individualized light aerobic training in human immunodeficiency virus infected patients with lipodystrophy and/or dyslipidemia.

BACKGROUND: The management of abdominal fat accumulation and metabolic disorders in HIV1-infected patients, by an aerobic training program, is considered. METHODS: Seventeen lipodystrophic and 2 dyslipidemic (without body modification) adults were studied before and after 4 months of training. The training load was individualized on a ventilatory threshold basis, determined during a maximal exercise test on cycle ergometer. Total (TAT), Visceral (VAT) and Subcutaneous Adipose Tissue (SAT) were assessed by CT-scan. Total (TC) and High Density Lipoprotein (HDL-C) Cholesterol, Triglycerides (TG), lactate (La), insulin and glucose were measured after a 12-hour-overnight fast. LDL, TC/HDL, TG/HDL, HOMA-insulin resistance index and coronary heart disease (CHD) relative risk (RR(CHD)) were calculated. RESULTS: Besides a significant improvement of aerobic fitness, trained patients exhibited a reduction in TAT (-12.8%, p < 0.001), specially at the visceral level (- 12%, p < 0.01) and in TC, TG and La (- 23%, - 43% and - 19% respectively, p < 0.01). HDL-C was increased (+ 6%, p < 0.01). All these effects were above changes that could be expected by a possible regression to the mean artefact. Both TC/HDL and TG/HDL were reduced (p < 0.01) and the estimated RR(CHD) decreased by approximately 13% (p < 0.01). No significant training effect was observed on the 9 available HOMAs. Significant correlations were found between changes in blood lipid values and baseline measures (r range - 0.55 to - 0.79, p < 0.05), indicating a larger improvement when baseline lipid parameters were higher. CONCLUSION: Aerobic training reduced visceral fat, lipid disorders, basal blood lactate and CHD markers in HIV patients. Training effects were particularly important for patients with marked dyslipidemia.

Does growth hormone treatment alter skeletal muscle mitochondrial respiration in rats?

OBJECTIVE: Growth hormone (GH) has been shown to stimulate lipolysis and enhance lipid oxidation. We investigated whether GH could improve mitochondrial oxidative capacity. METHOD: Fourteen male Wistar rats received 14-day treatment with biosynthetic human GH (10 IU/kg/24 h) or placebo. Mitochondria were isolated from the total muscle of one hind limb of the rat. Mitochondrial oxygen consumption was measured in vitro using a Clark-type electrode with three substrates: palmitoyl-L-carnitine, pyruvate and succinate (+ rotenone). RESULTS: Muscle mitochondrial yield was not significantly different in the GH-treated group from that in controls. Neither the basal nor ADP-stimulated respiratory state reached a significant difference between the 2 groups with palmitoyl-L-carnitine, pyruvate, and succinate. CONCLUSION: GH treatment did not improve the oxidative capacity of skeletal muscle mitochondria.

Insulin-like growth factor-binding protein 1 and blood rheology in athletes.

The GH-IGF axis has been recently suggested to modulate blood rheology in trained athletes, via GH effects on body water status and a possible action of IGF-I on erythrocyte deformability and aggregability. Another potential candidate for such a rheologic effect of the GH-IGF axis is insulin-like growth factor binding protein-1 (IGF-BP1) which is increased in trained people and correlated to fitness: IGF-BP1 is elevated in patients with polycythemia vera and stimulates erythroid burst formation in vitro. We investigated the statistical relationships between IGF-BP1 and blood rheology in athletes. 21 soccer players, age 24.5+/-1.13 yr; body mass index 23.7+/-0.38 kg/m(2); VO2max 44.8+/-7 ml.min(-1).kg(-1)). The major statistical determinant of IGFBP1 (measured at rest after overnight fast) was age (r=0.752, p=0.00013) which was not correlated with rheological parameters. IGF BP1 was negatively correlated with blood viscosity eta (high shear rate r=-0.516, p=0.024) and positively correlated with the percentage of extracellular water in total body water (ECW/TBW) (r=0.488, p=0.039). The previously reported correlations between IGF-I and both eta (r=0.637, p=0.003) and red cell rigidity "Tk" (r=0.696, p=0.0137) were observed, but IGF-I and IGF-BP1 were not correlated to each other (r=-0.176 ns) and their correlations with eta and Tk appeared to be independent when studied by multivariate analysis. Consistent with these correlations, subjects in the upper tertile of IGF-BP1 (>23.4 ng/ml) compared to those in the lower (<7.5 ng/ml) had a higher percentage of ECW/TBW (40.8+/-0.4 vs 38+/-0.8%, p=0.033), a lower eta (2.7+/-0.05 vs 2.97+/-0.06 mPa.s, p=0.016), and a lower Tk (0.54+/-0.05 vs 0.63+/-0.01, p=0.027). Thus, beside GH and IGF-I, IGF-BP1, which is reported to act on erythroid progenitors, exhibits statistical relationships with blood fluidity and erythrocyte flexibility that may suggest a physiological role in improving blood rheology.

Effect of hydration on exercise-induced growth hormone response.

DESIGN: Growth hormone (GH) has demonstrated water-retaining effects in subjects at rest, whereas other research has indicated that GH may stimulate sweating. Thus, the aim of this study was to investigate the effect of fluid intake on the exercise-induced GH response. METHODS: Seven healthy male volunteers (age: 27.4+/-1.3 years, weight: 74.5+/-1.1 kg, height: 179.3+/-2.3 cm) performed a 40-min submaximal rectangular cycling exercise in two different sessions. The first session (Session 1) was performed without water intake, and the second (Session 2) involved the ingestion of spring water (four intakes) corresponding to the volume of water lost during the first session. RESULTS: In session 1, the water loss was 568+/-32 ml. In Session 2, the volume of water loss was not significantly different from the volume of fluid intake (524+/-16 versus 568+/-32 ml respectively). The decrease in plasma volume was significantly reduced in Session 2 (-6.69+/-1.59% versus -11.3+/-1.89%; P<0.05). In Session 1, the GH concentration was significantly lower than that during Session 2 after 25 min (3.04+/-1.05 versus 5.26+/-1.81; P<0.05) and after 40 min (13.7+/-3.55 versus 17.60+/-4.14 ng/ml; P<0.05) of exercise. The total GH response was significantly lower in Session 1 than in Session 2 (136.6+/-39.2 versus 202.4+/-58.9 ng/ml x min; P<0.05). CONCLUSIONS: We conclude that the exercise-induced GH response decreases when exercise is performed without fluid intake.

Balance of substrate oxidation during submaximal exercise in lean and obese people.

OBJECTIVES: To compare fat and carbohydrate oxidation at different exercise intensities between overweight and normal-weight subjects, in order to analyze the influence of muscular metabolic abnormalities in obese people on substrate utilization during exercise. MATERIAL AND METHODS: 32 healthy sedentary overweight subjects (Body Mass Index (BMI): 30.8 +/- 0.8 kg/m(2); body fat: 37.4 +/- 1.1%; mean +/- SEM) and 26 controls (BMI: 23 +/- 0.4 kg/m(2); body fat: 22.7 +/- 1.1%) matched for age and sex were examined. The test consisted in four six-min. submaximal steady-state workloads with calculation of substrate oxidation rates and derived quantitative parameters, i.e., crossover point (defined as the power at which carbohydrate-derived energy becomes predominant) and maximal fat oxidation rate point. In addition, the accuracy of the test was analyzed and was found to be satisfactory. RESULTS: While exercise intensities were similar in both group, fat oxidation rates were significantly lower in overweight group (p<0.05). The crossover and the maximal fat oxidation rate points were significantly lower in overweight subjects than in controls: 33.3 +/- 2 vs 50.1 +/- 3.4% and 30.5 +/- 2.3 vs 44.6 +/- 3.3% of maximal aerobic power, respectively (p<0.001). CONCLUSION: Sedentary overweight subjects, compared to controls at the same exercise intensities, exhibited an alteration of the balance of substrate oxidation, reflected by lower rates of fat oxidation and a shift of quantitative parameters to lower intensities. The test appeared to be reliable and could be of interest to advise an individualized exercise prescription in obese people.

Exercise hypoglycemia in nondiabetic subjects.

Hypoglycemia during exercise is a common event due to an unbalance between training volume, nutrition, and external influences such as chronobiology, temperature or altitude, in subjects characterized by an acute and chronic increase in glucose effectiveness and insulin sensitivity. While it is preventable by adequate pre-exercise feeding with carbohydrates, it can also be induced by a prior carbohydrate meal with high glycemic index. Adequate training induces resistance to hypoglycemia via a shift in the balance of oxidized substrates and marked hormonal adaptations, but overtraining, by partially reversing this adaptation, favorizes hypoglycemia. Exercise hypoglycemia is a cause of fatigue or exercise cessation, but also impairs thermoregulatory adaptation and is assumed to fragilize muscles and tendons for traumatic events.

Postprandial reactive hypoglycemia.

Postprandial reactive hypoglycemia (PRH) can be diagnosed if sympathetic and neuroglucopenic symptoms develop concurrently with low blood sugar (<3.3 mmol). Neither the oral glucose tolerance test (OGTT) nor mixed meals are suitable for this diagnosis, due to respectively false positive and false negative results. They should be replaced by ambulatory glycemic control or, as recently proposed, an hyperglucidic breakfast test. PRH patients often suffer from an associated adrenergic hormone postprandial syndrome, with potential pathologic consequences such as cardiac arrhythmia. PRH could result from (a) an exaggerated insulin response, either related to insulin resistance or to increased glucagon-like-peptide 1; (b) renal glycosuria; (c) defects in glucagon response; (d) high insulin sensitivity, probably the most frequent cause (50-70%), which is not adequately compensated by hypoinsulinemia and thus cannot be measured by indices of insulin sensitivity such as the homeostatic model assessment. Such situations are frequent in very lean people, or after massive weight reduction, or in women with moderate lower body overweight. PRH is influenced by patient's alimentary habits (high carbohydrate-low fat diet, alcohol intake). Thus, diet remains the main treatment, although alpha-glucosidase inhibitors and some other drugs may be helpful.